We have observed that phagocytosis is stimulated early in P. berghei malaria but inhibited late in this lethal infection. We hypothesize that immune complexes, generated during malaria can either mediate or inhibit phagocytosis. We propose to isolate these complexes and determine their biologic activity and chemical nature. We will compare complexes isolated from lethal (P. berghei) and mild (P. yoelii yoelii) infections. In addition, the defects in spleen macrophage function during malaria will be studied by measuring adherence and phagocytosis to macrophage C3, FcRI and FcRII receptors.